ACIDOSIS IN SEVERE CHILDHOOD MALARIA

Data were prospectively collected on 306 Kenyan children, including bl ood gases in 258 (75%). Severe malaria caused a predominantly high-ani on-gap metabolic acidosis in at least 43% of children. Children with c oma and respiratory distress (CM+RD) had greater evidence of renal dys function, fewer mean pH and higher mean plasma osmolality than those w ith respiratory distress (RD) or coma (CM) as isolated findings (mean urea 10.7 vs. 6.0 vs. 4.3 mmol/l; mean creatinine 97 vs. 74 vs. 58 mu mol/l; mean osmolality 301 vs. 288 vs. 283 mosmol/l; and mean pH 7.16 vs. 7.29 vs. 7.39, respectively, p<0.001 for each comparison of CM+RD vs. RD or CM). In addition, children with CM+RD had a higher mean bloo d lactate (6.7 vs. 3.3 mmol/l, p<0.001), a lower mean haemoglobin (5.5 vs. 7.0 g/dl, p=0.002) and a lower mean age (26.4 vs. 41.9 months, p< 0.001) than children with CM and accounted for 15/24 (63%) of all deat hs. These and previous data implicate hypovolaemia and renal impairmen t in the pathogenesis of metabolic acidosis in severe childhood malari a. In children who are acidotic, anaemia is strongly associated with l actic acidaemia and may therefore contribute to its pathogenesis. Thes e data also imply that coma in acidotic children (CM+RD) and those wit h an isolated encephalopathy (CM) may result from quite different path ophysiological mechanisms.